Adverse Effects Of Carbamazepine Research Articles

Carbamazepine overdose presenting as a diabetes insipidus –like condition in a child

overdoses it can produce various side effects involving neurological, cardiac, hematological and endocrinal systems. Inappropriate secretion of Anti Diuretic Hormone (ADH) is a well-known complication of carbamazepine toxicity. We are reporting an unusual complication in an adolescent girl with intentional carbamazepine overdose. A sixteen year old female with carbamazepine ingestion presented to our hospital with altered sensorium. On admission she was found to have a very high serum carbamazepine level and metabolic acidosis. In contrast to the possible inappropriate secretion of ADH, as an adverse effect of carbamazepine, her hospital course was complicated with a diabetes insipidus – like condition following treatment with multiple doses of activated charcoal and sodium bicarbonate therapy.

Adverse effects of carbamazepine, phenytoin, valproate and lamotrigine monotherapy in epileptic adult Chinese patients

Antiepileptic drugs (AEDs) have been widely used in patients with epilepsy but the adverse effects in adult Chinese patients have not been investigated. This study evaluated the adverse effects of four commonly prescribed AED monotherapies with carbamazepine (CBZ), phenytoin (PHT), valproate (VPA), and lamotrigine (LTG) in adult Chinese patients with epilepsy. The prospective open-label clinical trial was conducted at the Chongqing Epilepsy Center. The study enrolled 505 adults with newly diagnosed epilepsy, including generalized tonic-clonic (n=110), partial and partial secondarily generalized (n=395) seizures. Patients were evaluated by two clinicians at the Center and were prescribed one type of AED monotherapy with CBZ, PHT, VPA or LTG for a 24-month period. An adverse effect profile, as well as efficacy of monotherapy, was obtained through a face-to-face interview with the patient at each visit. A physical examination and routine laboratory tests were performed during a clinical screening. A total of 62.6% (316/505) patients successfully completed the AED monotherapy study: 64.3% of those receiving CBZ, 55.9%--PHT, 61.5%--VPA, and 66.2%--LTG. However, 34.7% of the patients discontinued the AED monotherapy because of unsatisfactory seizure control. Overall, 18% of patients experienced adverse effects: for CBZ (25/168; 14.9%), PHT (18/59; 30.5%), VPA (32/192; 16.7%) and LTG (16/86; 18.6%). The most common drug-related adverse events included gastrointestinal disturbances, loss of appetite and nausea, weight gain and fatigue/tiredness. Tremor and nystagmus occurred in some patients receiving PHT and VPA. Two CBZ, one PHT and four LTG patients (n=7) discontinued the study due to rash. Adult Chinese patients with epilepsy accepted and tolerated monotherapy with CBZ, PHT, VPA, and LTG. No fatal adverse events occurred. Unsatisfactory seizure control was a primary reason for withdrawal from the AED monotherapy study.

Effect of arachidonyl-2′-chloroethylamide, a selective cannabinoid CB1 receptor agonist, on the protective action of the various antiepileptic drugs in the mouse maximal electroshock-induced seizure model

The aim of this study was to determine the influence of arachidonyl-2'-chloroethylamide (ACEA - a highly selective cannabinoid type 1 [CB1] receptor agonist) on the protective action and acute adverse effects of carbamazepine, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, and topiramate in the maximal electroshock seizure model and chimney test in mice. Tonic hind limb extension (seizure activity) was evoked in adult male albino Swiss mice by a current (sine-wave, 25 mA, 500 V, 50 Hz, 0.2s stimulus duration) delivered via auricular electrodes. Acute adverse-effect profiles of the studied antiepileptic drugs with respect to motor coordination was assessed in the chimney test. Additionally, long-term memory and skeletal muscular strength were measured along with free plasma (non-protein bound) and total brain antiepileptic drug concentrations. To inhibit the rapid metabolic degradation of ACEA by the fatty-acid amide hydrolase, phenylmethylsulfonyl fluoride (PMSF) was used at a constant ineffective dose of 30 mg/kg. Results indicate that ACEA (2.5 mg/kg, i.p.) co-administered with PMSF (30 mg/kg, i.p.), significantly enhanced the anticonvulsant activity of phenobarbital, but not that of carbamazepine, lamotrigine, oxcarbazepine, phenytoin, or topiramate in the maximal electroshock seizure test in mice. Moreover, ACEA (2.5 mg/kg) with PMSF (30 mg/kg) had no significant impact on the acute adverse effects of all examined antiepileptic drugs in the chimney test in mice. The protective index values (as quotients of the respective TD(50) and ED(50) values denoted from the chimney and maximal electroshock seizure tests, respectively) for the combinations of ACEA (2.5 mg/kg) and PMSF (30 mg/kg) with carbamazepine, oxcarbazepine, phenobarbital, and topiramate were greater than those denoted for the antiepileptic drugs administered alone. Only, the protective index values for the combination of ACEA (2.5 mg/kg) and PMSF (30 mg/kg) with lamotrigine and phenytoin were lower than those determined for the antiepileptic drugs administered alone. Pharmacokinetic experiments revealed that ACEA (2.5 mg/kg) and PMSF (30 mg/kg) affected neither free plasma (non-protein bound) nor total brain concentrations of phenobarbital in mice. Moreover, ACEA and PMSF in combination with carbamazepine, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, and topiramate did not alter long-term memory or skeletal muscular strength in experimental animals. In conclusion, the enhanced anticonvulsant action of phenobarbital by ACEA and PMSF, lack of pharmacokinetic interaction and no acute adverse effects between the examined compounds, make the combination of ACEA and PMSF with phenobarbital of pivotal importance for further experimental and clinical studies. The combinations of ACEA and PMSF with carbamazepine, lamotrigine, oxcarbazepine, phenytoin, and topiramate are neutral from a preclinical viewpoint.

Treatment of post-herpetic pain in myasthenia gravis: exacerbation of weakness due to gabapentin

Here, we present a case of a 64-year-old female suffering from a severe form of antibody-positive myasthenia gravis. Under an immunosuppressive regimen with cyclosporine A, she experienced an episode of thoracic herpes zoster followed by intense post-herpetic neuralgia. In order to avoid drug interactions as well as adverse effects of carbamazepine in myasthenia gravis, gabapentin was chosen for the treatment of neuropathic pain. Within a few days she noticed increasing weakness, but continued medication for 8 weeks as gabapentin was not identified as the hazardous agent by her physician. Acetylcholine receptor antibody levels remained unchanged, but increased decrement was observed clinically and in repetitive nerve stimulation. After withdrawal of gabapentin, she recovered quickly to her previous condition.

Investigation and medical management of trigeminal neuralgia byconsultant oral and maxillofacial surgeons in the British Isles

Trigeminal neuralgia is an extremely painful affliction of the face that is treated by various specialists including oral and maxillofacial surgeons. Some aspects of its management remain controversial, including screening for secondary trigeminal neura lgia, and the monitoring of treatment with carbamazepine. There is, however, little information available about current practice. A postal questionnaire was sent to 254 fellows of the British Association of Oral and Maxillofacial Surgeons (BAOMS) about v arious aspects of the management of trigeminal neuralgia. One hundred and seventy nine replies (70%) were received. Orofacial and cranial nerve examinations were undertaken by the majority of surgeons, but most did not routinely arrange computed tomograp hy or magnetic resonance imaging for all patients, nor did they refer the patient to a neurologist. In contrast with current recommendations, warnings about the adverse effects of carbamazepine were given by only a few surgeons, while most routinely moni tored full blood counts.

Carbamazepine-Induced Systemic Lupus Erythematosus

A 21-year-old woman suffering from bipolar affective disorder developed systemic lupus erythematosus (SLE) with characteristic laboratory findings, 18 months after starting carbamazepine maintenance treatment. SLE receded after withdrawal of carbamazepine and treatment with anti-inflammatory drugs. Although both the spontaneous occurrence of SLE and the psychosis as a sign of CNS involvement of SLE cannot be excluded, SLE could be considered as an adverse effect of carbamazepine.

Carbamazepine-induced constipation

We report three patients who developed constipation as an adverse effect of carbamazepine (CBZ) therapy. Constipation occurred within a few days of CBZ introduction, resolved after CBZ discontinuation, and was not dose-responsive. It was refractory to the concomitant use of oral laxatives in two cases, necessitating CBZ discontinuation. In a third patient, constipation was controlled by a fiber agent, allowing continuation of CBZ therapy. Potential mechanisms for this idiosyncratic, poorly reported adverse event are discussed.